Research Article
Inhibition of PLK3 Attenuates Tubular Epithelial Cell Apoptosis after Renal Ischemia–Reperfusion Injury by Blocking the ATM/P53-Mediated DNA Damage Response
Figure 5
Oxidative stress and the DDR were induced during H/R injury in TECs and I/R injury in mouse kidneys. HK-2 cells were subjected to normoxia or hypoxia for 24 h/reoxygenation for 6 h. C57BL/6J male mice were subjected to sham operation or 30 min of bilateral renal ischemia, followed by 24 h of reperfusion. (a and b) MDA levels and SOD activity in renal cortex homogenates were analyzed. (c and d) Flow cytometric analysis of H2DCFH-DA staining and cytofluorometric analysis of DHE staining were performed to measure the levels of cellular ROS production after H/R treatment (; magnification, 400x). (e) Representative images of immunofluorescence staining of γH2AX in TECs (; magnification, 400x). (f) The expression of DNA damage-related proteins was measured by Western blot after H/R injury. (g) PLK3 mRNA levels in the H2O2-induced oxidative stress model. (h) PLK3 protein levels after H2O2 stimulation. The data are presented as the . . , , , and . DHE: dihydroethidium; MDA: malondialdehyde; SOD: superoxide dismutase.
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